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Increased Expression of VCAM1 on Brain Endothelial Cells Drives Blood-Brain Barrier Impairment Following Chronic
Huiwen Zhang1, Junkui Shang1, Wei Li1
1Department of Neurology, Zhengzhou University People's Hospital, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, China.
ACS Chemical Neuroscience
|May 6, 2024
Summary
Vascular dementia involves blood-brain barrier (BBB) dysfunction. Researchers found increased vascular cell adhesion molecule 1 (VCAM1) expression in chronic cerebral hypoperfusion models, suggesting VCAM1 blockage as a potential treatment for neurodegenerative diseases.
Area of Science:
- Neuroscience
- Pathology
- Biomedical Engineering
Background:
- Chronic cerebral hypoperfusion (CCH) causes blood-brain barrier (BBB) dysfunction, a key factor in vascular dementia (VD).
- The molecular mechanisms underlying BBB impairment in VD are not fully understood.
- Vascular cell adhesion molecule 1 (VCAM1) is implicated in BBB regulation.
Purpose of the Study:
- To investigate the role of VCAM1 in BBB dysfunction in a CCH-induced VD model.
- To explore VCAM1 as a potential therapeutic target for VD.
Main Methods:
- Utilized a CCH-induced VD mouse model.
- Quantified VCAM1 expression in brain endothelial cells (ECs).
- Assessed BBB leakage and white matter integrity.
- Administered a VCAM1 inhibitor (K-7174).
Main Results:
- Elevated VCAM1 expression was observed in ECs of the VD model.
- VCAM1 expression correlated with BBB impairment severity and white matter lesions.
- Inhibition of VCAM1 (K-7174) reduced BBB leakage and protected white matter.
- Pharmacological BBB manipulation did not alter VCAM1 expression.
Conclusions:
- VCAM1 is a critical regulator of BBB dysfunction in CCH-induced VD.
- Blocking VCAM1 offers a promising therapeutic strategy for CCH-related neurodegenerative diseases.
